title: The role of Th17/Tc17 peripheral blood T cells in psoriasis and their positive therapeutic response.
abstract: It is known that NB-UVB therapy can suppress a broad range of immune cells, but the additional effect of bathing in geothermal seawater still remains unclear. To study the influence of treatment on the expression of circulating immune cells contributing to the pathogenesis of psoriasis, six patients with psoriasis were treated with bathing in geothermal seawater two times daily combined with NB-UVB five times/week for 2 weeks and six patients were treated with NB-UVB therapy three times/week for 8 weeks. Disease severity (Psoriasis Area and Severity Index, PASI), chemokines, inflammatory cytokines, T cells and Toll-like receptors in the blood and skin samples were evaluated on enrolment (W0) and at 1 (W1), 3 (W3) and 8 (W8) weeks. Compared with healthy controls, psoriasis patients with active disease had significantly higher proportion of peripheral CLA+ T cells expressing CCR10 and CD103 and T cells with both Th1/Tc1 (CD4+/CD8+ IFN-γ+ or TNF-α+ cells) and Th17/Tc17 (CD4+CD45R0+IL-23R+, CD4+/CD8+ IL-17A+ or IL-22+ cells) phenotypes. Both treatments gave a significant clinical effect; however, bathing in geothermal seawater combined with NB-UVB therapy was more effective than NB-UVB therapy alone. This clinical improvement was reflected by a reduction in circulating CLA+ peripheral blood T cells and by a decreased Th1/Th17 and Tc1/Tc17 inflammatory response. These findings suggest that the inflammatory response in psoriasis is predominantly driven by both CD4+ and CD8+ skin-homing tissue retaining T cells of the Th17/Tc17 lineages.
authors.affiliation: Department of Medicine, University of Iceland, Reykjavík, Iceland; Department of Dermatology, Landspitali-University Hospital, Reykjavík, Iceland; Department of Immunology, Landspitali-University Hospital, Reykjavík, Iceland.
authors.forename: J H
authors.initials: JH
authors.lastname: Eysteinsdóttir
authors.forename: B
authors.initials: B
authors.lastname: Sigurgeirsson
authors.forename: J H
authors.initials: JH
authors.lastname: Ólafsson
authors.forename: Th
authors.initials: T
authors.lastname: Fridriksson
authors.forename: B A
authors.initials: BA
authors.lastname: Agnarsson
authors.forename: S
authors.initials: S
authors.lastname: Davíðsson
authors.forename: H
authors.initials: H
authors.lastname: Valdimarsson
authors.forename: B R
authors.initials: BR
authors.lastname: Lúðvíksson
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D001494:Baths; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D018450:Disease Progression; D005260:Female; D045482:Hot Springs; D006801:Humans; D039001:Integrin alpha Chains / Q000378:metabolism; D007371:Interferon-gamma / Q000097:blood; D020381:Interleukin-17 / Q000097:blood; D007378:Interleukins / Q000097:blood; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D011565:Psoriasis / Q000276:immunology* / Q000532:radiotherapy / Q000628:therapy*; D054447:Receptors, CCR10 / Q000378:metabolism; D012623:Seawater; D012867:Skin / Q000166:cytology / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology*; D051193:Toll-Like Receptors / Q000097:blood; D014467:Ultraviolet Therapy / Q000379:methods*; D000097043:Interleukin-22
chemical_list: D015703:Antigens, CD; D039001:Integrin alpha Chains; D007371:Interferon-gamma; D020381:Interleukin-17; D007378:Interleukins; D054447:Receptors, CCR10; D051193:Toll-Like Receptors; D000097043:Interleukin-22; C515706:CCR10 protein, human; C091367:alpha E integrins